Paraplegia- causes, localisation

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Paraplegia — Causes & Localisation

Definition

Paraplegia is paralysis (complete or incomplete) of both lower limbs. It results from interruption of descending corticospinal tracts or of motor neurons/peripheral nerves supplying the legs.
An injury below T1 causes paraplegia; above T1 (cervical cord) causes tetraplegia/quadriplegia. An injury in the upper cervical cord can cause death by denervating the diaphragm. — Gray's Anatomy for Students

Localisation of the Lesion

The clinically important distinction is between spinal cord, nerve root, and peripheral nerve lesions.

1. Spinal Cord (most common site)

FeatureFinding
Level of weaknessAll muscles below the lesion level
Sensory lossCircumferential sensory level on trunk (spinothalamic + posterior column involvement)
Reflexes (acute)Flaccid paralysis + areflexia (spinal shock)
Reflexes (chronic)Spastic paraplegia, hyperreflexia, bilateral Babinski signs, extensor/flexor spasms
AutonomicBladder & bowel dysfunction (initially atonic → later spastic), anhidrosis below level, orthostatic hypotension
Segmental LMN signsAt the level of the lesion: atrophy, areflexia, fasciculations (anterior horn / root damage)
"With acute lesions, the paralysis is flaccid as a result of spinal cord hypoexcitability (spinal shock). Eventually, hypertonic, hyperreflexic paraplegia develops with bilateral Babinski signs." — Localization in Clinical Neurology, 8e
Level clues:
  • Above T6 → risk of autonomic dysreflexia (severe uncontrolled hypertension)
  • Cervicothoracic sympathetic chain involved → ipsilateral Horner syndrome
  • Complete lower cord lesion → flexion at hips and knees; high/incomplete cord lesion → extension at hips and knees

2. Cauda Equina / Conus Medullaris

FeatureFinding
WeaknessFlaccid, lower motor neuron (LMN) type
ReflexesAbsent (areflexia)
SensorySaddle anaesthesia, asymmetric radicular pattern
Bladder/bowelAtonic (overflow incontinence)

3. Peripheral Nerve Disease

  • Motor loss is distal > proximal (mainly legs)
  • Sphincter function usually spared
  • Sensory loss is distal and often modality-selective
  • Exceptions: Guillain-Barré syndrome, diabetic neuropathy, porphyria (more proximal involvement) — Adams and Victor's Principles of Neurology, 12e

Causes of Paraplegia

Acute Onset (minutes to hours)

CauseNotes
Spinal cord traumaMost common cause — fracture-dislocation of spine
Spinal cord infarctionAnterior spinal artery occlusion; segmental aortic branch occlusion (dissecting aneurysm, atheroma, vasculitis, nucleus pulposus embolism)
Vascular malformation / dural AV fistulaCord ischaemia by complex mechanism
Epidural/subdural haemorrhageHaemorrhagic diathesis, warfarin; rarely post-lumbar puncture

Subacute Onset (hours to days)

CauseNotes
Postinfectious myelitisDemyelinating or necrotising myelopathy
Epidural abscessBacterial; cord compression
Epidural tumourCord compression
Paralytic poliomyelitisPurely motor, mild meningitis
Guillain-Barré syndromePredominantly motor, ascending, often with sensory disturbance

Chronic / Progressive Onset

CauseNotes
Multiple sclerosisMost common cause of chronic spinal paraplegia in adults
Spinal tumour (intrinsic or extrinsic)Intramedullary or extramedullary
Cervical spondylosis / disc prolapseEspecially with congenitally narrow canal
Subacute combined degenerationVitamin B12 or copper deficiency — posterior + lateral columns
SyringomyeliaCentral cord cavitation
Epidural abscess (chronic)Tuberculous, fungal, granulomatous
Syphilitic meningomyelitis
HIV myelopathy / HTLV-1Tropical spastic paraparesis (HTLV-1)
Motor neuron disease (ALS)Corticospinal tract degeneration
Neuromyelitis optica (NMO)Aquaporin-4 antibody; severe transverse myelitis
Epidural lipomatosisUsually steroid-related
Hereditary spastic paraplegiaGenetic — upper motor neuron degeneration
Degenerative lateral & posterior column disease

Infantile / Congenital

CauseNotes
Periventricular leukomalaciaMost common cause of infantile diplegia (spastic legs > arms)
Congenital cysts / tumours / diastematomyelia
Spinal cord infarctionUmbilical catheter thrombotic complication
Metabolic cerebral diseasesLeukodystrophies, lipid storage diseases
Adams and Victor's Principles of Neurology, 12e; Localization in Clinical Neurology, 8e

Key Localisation Summary

Lesion SitePatternToneReflexesSphincters
Spinal cord (acute)Below levelFlaccid (shock)Absent → briskImpaired
Spinal cord (chronic)Below levelSpasticHyperreflexic, BabinskiImpaired
Conus medullarisSaddle + legsFlaccidAbsentAtonic
Cauda equinaAsymmetric radicularFlaccidAbsentVariable
Peripheral nerveDistal legsFlaccidAbsent/reducedUsually spared
Bilateral cortex / parasagittalLegs > arms (diplegia)SpasticHyperreflexicVariable

Paraparesis

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Paraparesis

Paraparesis is partial (incomplete) weakness of both lower limbs, in contrast to paraplegia which implies complete paralysis. The distinction is clinically important because paraparesis often represents a reversible or treatable condition.

Definition & Clinical Features

Spasticity of both legs gives rise to a spastic paraparesis: the legs are stiffly extended at the knees, plantarflexed at the ankles, and slightly flexed at the hips. Both legs circumduct, and the toes catch on the floor with each step. The gait is slow and laboured. When the disorder begins in childhood, there is a tendency to adduct the legs — the classic "scissors gait."Bradley and Daroff's Neurology in Clinical Practice

Classification

A. Spastic Paraparesis (UMN type)

Lesion in the corticospinal tracts — bilateral, above the level of the lumbar cord.
Features:
  • Increased tone (spasticity), hyperreflexia, clonus
  • Bilateral extensor plantar responses (Babinski sign)
  • Weakness below the level of the lesion
  • Bladder/bowel dysfunction
  • Sensory level on trunk (if spinal cord)
Causes:
CategoryExamples
Degenerative / StructuralCervical spondylotic myelopathy (most common cause of spastic paraparesis in patients >55 years), lumbar spondylosis, disc prolapse
DemyelinatingMultiple sclerosis, neuromyelitis optica (NMO)
VascularAnterior spinal artery infarction, spinal AV fistula/malformation
InfectiveHTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP), HIV myelopathy, syphilitic meningomyelitis, epidural abscess (TB, bacterial)
NeoplasticSpinal cord compression by extradural tumour (metastasis), intradural extramedullary (meningioma, neurofibroma), intramedullary tumour
Nutritional / MetabolicSubacute combined degeneration (B12/copper deficiency — posterior + lateral columns)
HereditaryHereditary spastic paraplegia (HSP) — pure form: progressive spasticity, arms and sphincters unaffected; little or no actual weakness
InflammatoryTransverse myelitis (post-infectious, autoimmune)
Structural malformationsSyringomyelia, Arnold-Chiari malformation
Parasagittal / bilateral corticalParasagittal meningioma, bilateral anterior cerebral artery territory strokes (legs > arms)
"Cervical spondylotic myelopathy causes the greatest degree of impairment and disability in the continuum of spondylosis. In addition, myelopathy is the most common cause of spastic paraparesis in patients older [than 55]." — Tintinalli's Emergency Medicine

B. Flaccid Paraparesis (LMN type)

Lesion in the lower motor neurons, nerve roots, or peripheral nerves.
Features:
  • Decreased or absent tone
  • Areflexia or hyporeflexia
  • Muscle wasting, fasciculations
  • Sensory loss in radicular or "stocking" distribution
  • Sphincters variably affected
Causes:
CategoryExamples
Cauda equina syndromeCentral disc prolapse (L4/5, L5/S1), epidural tumour, spinal stenosis
Conus medullaris lesionTumour, AVM, infarction
Guillain-Barré syndromeAscending, predominantly motor; post-infectious
PolyneuropathyDiabetic, CIDP, toxic (heavy metals), paraneoplastic
Motor neuron diseaseLower motor neuron variant; primary lateral sclerosis (UMN)
PoliomyelitisPure LMN; anterior horn cell destruction

Key Distinguishing Features: UMN vs LMN Paraparesis

FeatureSpastic (UMN)Flaccid (LMN)
ToneIncreased (spasticity)Decreased (flaccidity)
ReflexesHyperreflexic, clonusHyporeflexic / absent
Plantar responseExtensor (Babinski +ve)Flexor or absent
WastingMild/lateEarly and prominent
FasciculationsAbsentMay be present
Sensory levelTruncal level (cord)Saddle/radicular/glove-stocking
BladderSpastic (urgency)Atonic (retention/overflow)

Important Mimics

  • Bilateral leg dystonia (dystonic paraparesis): mimics spastic paraparesis; occurs in dopa-responsive dystonia in childhood. Can be misdiagnosed as HSP or cerebral diplegia. A "striatal toe" (spontaneous great toe extension) may be misinterpreted as Babinski.
  • Distinction is critical: levodopa is curative in dopa-responsive dystonia.
"Occasionally bilateral leg dystonia (dystonic paraparesis) mimics a spastic paraparesis... Clinical differentiation between these conditions can be difficult. Brisk tendon reflexes occur in both." — Bradley and Daroff's Neurology in Clinical Practice

Investigation Approach

  • MRI spine (with contrast): investigation of choice — exclude compressive, inflammatory, vascular, and demyelinating myelopathy
  • MRI brain: parasagittal lesions, MS plaques
  • CSF analysis: oligoclonal bands (MS), infection, inflammatory markers
  • Serum B12, copper, folate: subacute combined degeneration
  • HTLV-1 serology: in endemic regions or at-risk patients
  • HIV serology
  • VEPs, SSEPs: demyelination
  • Genetic testing: hereditary spastic paraplegia (SPG gene panel)
  • EMG/NCS: to differentiate from peripheral neuropathy or polyradiculopathy
"Patients with paraparesis of recent onset should be investigated with MRI of the spinal cord to exclude potentially treatable causes such as spinal cord compression." — Bradley and Daroff's Neurology in Clinical Practice
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